Equol
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It can also pass cellular membranes, so it can enter the prostate and hair follicles and attach itself to DHT there. A few studies have confirmed that DHT levels are lowered.Comment
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It does lower the amount of serum DHT, just with a different method to fin. Fin stops the production of DHT by blocking 5a. Equol attaches itself strongly to DHT, after which it is no longer DHT.
It can also pass cellular membranes, so it can enter the prostate and hair follicles and attach itself to DHT there. A few studies have confirmed that DHT levels are lowered.Comment
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If DHT levels are lowered wont the body compensate by producing more test? And if 5AR is the same more test will be converted to DHT, requiring more and more equol. I also dont see how this method mitigates the sides experienced during the use of Fin... just looks like a different version of fin - might aswel call it "Dutasteride II".
just asking.Comment
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If DHT levels are lowered wont the body compensate by producing more test? And if 5AR is the same more test will be converted to DHT, requiring more and more equol. I also dont see how this method mitigates the sides experienced during the use of Fin... just looks like a different version of fin - might aswel call it "Dutasteride II".
The body needs to convert a certain amount of free T to DHT. Excess T? By blocking 5ar...the body is not able to do so, and therefore T levels rise.
Equol allows the conversion from T to DHT, which the body needs. That in itself makes it potentially safer than Fin.
Equol producers have a significantly low incidence rate of prostate cancer. Fin was originally produced for the prostate. Prostate cancer is highly dependant on DHT attaching to receptors.
Ausio Pharmaceuticals claim to have tested equol upto 320mg safely, albeit for a short period. they are currently testing it in men upto 150mg for prostate health.
These studies in healthy participants establish the first report on the plasma and urine levels of unconjugated S-equol after oral dosing. The rapid absorption and pharmacokinetic parameters show that S-equol exposure is linear with dose. There were no significant drug-related adverse events even at …
What people need to understand that there is a huge difference in blocking 5ar and de-activating just DHT. Though the outcome is the same, the mechanism will get very different reactions from the body.
blocking 5ar effects more than just DHT. 5ar does MORE than just converting T to DHT. The body needs this process of T to DHT. if its not able to do this, T levels rise.
"In vivo equol treatment significantly decreased rat prostate weights and serum 5alpha-DHT levels but did not alter LH, testosterone, and estradiol levels"
Now this is for rats of course. But I have read other studies indicating the same. This all suggests that it is the blocking of 5ar that effects T levels, not the drop in DHT levels. Now, noone knows for sure, which is why Equol deserves more attention.
I believe T levels will be effected somewhat, and probably varies from person to person. But i have no doubt that blocking 5ar is more harmful than de-activating just DHT. Lets be realistic, everything has some side effect. We're talking about the possibility of equol being FAR MORE safer than fin.
Thats my non expert opinion on it.Comment
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testosterone/dht/5ar reductase is not the problem. excess of these IS the problem.
dht/androgens regulate the hair cycle through expression of cox2 and possibly other unknown enzymes which are involved in the hair cycle.
so therefore people with excess of either andorgens/5ar enzymes would exccessiveley shed hair through -> excess cox2 initiated via androgens -> this would show up as thinning/balndess
people with "normal levels" of androgens/5ar would cycle hair in a way that baldness/thinning/minutuarisation is not viewable
The reason why people with "normal levels" of androgens do not experience minutuarising hairs is that their cox 2 levels downregulate during regeneration.
find a way to block/lower cox2 and you would stop hair shedding/baldness dead in its tracks.Comment
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testosterone/dht/5ar reductase is not the problem. excess of these IS the problem.
dht/androgens regulate the hair cycle through expression of cox2 and possibly other unknown enzymes which are involved in the hair cycle.
so therefore people with excess of either andorgens/5ar enzymes would exccessiveley shed hair through -> excess cox2 initiated via androgens -> this would show up as thinning/balndess
people with "normal levels" of androgens/5ar would cycle hair in a way that baldness/thinning/minutuarisation is not viewable
The reason why people with "normal levels" of androgens do not experience minutuarising hairs is that their cox 2 levels downregulate during regeneration.
find a way to block/lower cox2 and you would stop hair shedding/baldness dead in its tracks.Comment
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its possible the "point of no return" does not exist and in actual fact -> time and cox2 blocking will likeley regernarate your hair including stopping you from going bald.Comment
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either directly lower cox 2 or indirectly -> lower dht to acceptable levels having the knock on effect on cox 2 expression.
sulfasalzine, benaxoprofen, curcumin, saw palmetto (certain brands), 9 grams MSM, and im sure theres many many stuff out there that does this potently i.e someone needs to trial d-flame supplement to see if it has any effect on hair.
propecia may be the fda approved way to go but certainly not a wise decsion IMO.Comment
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either directly lower cox 2 or indirectly -> lower dht to acceptable levels having the knock on effect on cox 2 expression.
sulfasalzine, benaxoprofen, curcumin, saw palmetto (certain brands), 9 grams MSM, and im sure theres many many stuff out there that does this potently i.e someone needs to trial d-flame supplement to see if it has any effect on hair.
propecia may be the fda approved way to go but certainly not a wise decsion IMO.
Also, i dont see how an oral cox 2 suppressor is a good choice. If we took oral medicine strong enough to block cox 2 in the scalp, would that not be massively dangerous for us?Comment
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